Sickle cell anemia patients do not become anemic until hemoglobin F production ceases in neonatal life. Hydroyurea stimulates Hgb F production. This study will examine the pharmacology of hydroxyurea in patients with sickle cell anemia, quantitate the effect of hydroxyurea on the amount of Hgb F in their red cells, and determine whether the Hgb F levels achieved when the drug is given to these patients are clinically significant.